OBJECTIVE: To study the level of circulating Alarin in obese children and its association with various metabolic parameters. METHODS: A total of 86 obese children with a body mass index (BMI) above the 95th percentile were enrolled as the obesity group, and 82 healthy children, matched for age and sex, with a BMI below the 85th percentile were enrolled as the healthy control group. According to the presence or absence of insulin resistance (IR), the obesity group was further divided into an IR group with 27 children and a non-IR group with 59 children. Related anthropometric parameters, including body height, body weight, systolic blood pressure (SBP), and diastolic blood pressure (DBP), were measured, and BMI was calculated. Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), uric acid (UA), fasting insulin (FINS), and fasting blood glucose (FBG) were measured. The area under the receiver operating characteristic curve (AUC) for glucose and insulin, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), and whole-body insulin sensitivity index (WBISI) were calculated. ELISA was used to measure the level of circulating Alarin. RESULTS: The obesity group had a significantly higher level of circulating Alarin than the healthy control group (P<0.01). The IR group had a significantly higher level of circulating Alarin than the non-IR group (P<0.01). Circulating Alarin was positively correlated with BMI, TG, FBG, AUC-glucose, AUC-FINS, and HOMA-IR (P<0.05) and was negatively correlated with WBISI (P<0.05). The circulating Alarin level had a linear regression relationship with BMI, FBG, and HOMA-IR, among which HOMA-IR had the greatest influence on the circulating Alarin level (P<0.05). CONCLUSIONS There is a significant increase in the circulating Alarin level in obese children, which may be associated with the development of obesity and IR.
Blood Glucose ; Body Mass Index ; Child ; Galanin-Like Peptide ; Humans ; Insulin ; Insulin Resistance ; Obesity

The nutritional and metabolic status alters the peripheral taste perception and food intake by participating in the modulation of taste information integration. The taste receptors and neuropeptides in the taste buds are the important targets of this modulation process. To explore the effects of nutritional status on the expressions of galanin and its receptors in the taste buds, we compared the mRNA levels of galanin and its specific receptor GalR2 in the taste buds among the high-fat diet induced obese rats (HF), chronically restricted diet rats (CR) and control rats. The high-fat diet, half of chow diet, and normal chow diet were given to HF, CR and control groups for 6 weeks, respectively. The body weight and some metabolic indexes, including blood glucose, triglyceride and cholesterol levels were detected. The mRNA expressions of galanin and its receptors in taste buds were determined using real-time PCR. Results showed that compared with control rats, the body weights, levels of blood glucose and triglyceride were significantly elevated in HF rats; while the mRNA expressions of galanin and GalR2 were dramatically decreased. However, galanin mRNA expression in CR rats was increased to 2.3 times of that in control group. Considering the results obtained from our previous studies, we conclude that the behavioral changes in tasting choice of HF rats may be related to the expressions of galanin and GalR2 in the taste buds. The changes of galanin and GalR2 in taste buds are involved in the peripheral mechanism of nutritional status regulating taste perception and feeding behavior in rats.
Animals ; Body Weight ; Galanin ; metabolism ; Nutritional Status ; RNA, Messenger ; metabolism ; Rats ; Receptor, Galanin, Type 2 ; metabolism ; Taste Buds ; metabolism

Stroke leads to a variety of pathophysiological conditions such as ischemic infarct, cerebral inflammation, neuronal damage, cognitive decline, and depression. Many endeavors have been tried to find the therapeutic solutions to attenuate severe neuropathogenesis after stroke. Several studies have reported that a decrease in the neuropeptide regulator ‘galanin’ is associated with neuronal loss, learning and memory dysfunctions, and depression following a stroke. The present review summarized recent evidences on the function and the therapeutic potential of galanin in post-ischemic stroke to provide a further understanding of galanin's role. Hence, we suggest that galanin needs to be considered as a therapeutic factor in the alleviation of post-stroke pathologies.
Depression ; Galanin ; Inflammation ; Learning ; Memory ; Neurons ; Neuropeptides ; Pathology ; Stroke

Development of various antidepressants such as monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin norepinephrine reuptake inhibitors, and noradrenergic and specific serotonergic antidepressant has led to a tremendous progression of pharmaceutical treatment for depression, but still there are some limitations of current antidepressants, such as treatment-resistant depression and delayed onset of antidepressants. The pathogenesis of depression is unclear because depression is a heterogeneous disease state, and the mechanisms of antidepressants remain uncertain as well. Nevertheless, in an attempt to develop novel antidepressants, some trials have been conducted based on the potential biological mechanism discovered in the numerous research results. This review will provide information about the potential novel antidepressants and the current states of clinical studies using them. In particular, some potential novel antidepressants anti-inflammatory agents, antioxidants, anticholinergics, modulators of Hypothalamic Pituitary Adrenal Axis, glutamate, and opioid systems, as well as some neuropeptides such as susbstance P, neuropeptide Y, and galanin will be discussed.
Anti-Inflammatory Agents ; Antidepressive Agents ; Antidepressive Agents, Tricyclic ; Antioxidants ; Axis, Cervical Vertebra ; Cholinergic Antagonists ; Depression* ; Depressive Disorder ; Drug Therapy ; Galanin ; Glutamic Acid ; Monoamine Oxidase Inhibitors ; Neuropeptide Y ; Neuropeptides ; Norepinephrine ; Serotonin ; Serotonin Uptake Inhibitors

OBJECTIVETo construct an N-2a cell line stably expressing PcDNA 3.1-platelet derived growth factor-galanin (GAL) and explore the effect of over-expressed GAL on proliferation and apoptosis of N-2a cell in vitro.

METHODSThe vector containing the target gene was transfected into N-2a cells by liposome, and cell clones stably over-expressing GAL was obtained via G418 screening. GAL mRNA and protein levels were determined by reverse transcriotion-polymerase chain reaction (RT-PCR) and Western blot. The proliferation of N-2a cells was detected by MTT.The cell cycle and apoptosis were detected by flow cytometry.

RESULTSRT-PCT and Western blot indicated that GAL genes were highly expressed in the transfected N-2a cells (i.e.GAL-N-2a). As shown by MTT, the proliferation of the N-2a cells transfected with PcDNA 3.1-PDGF-GAL was significantly slower than the control group(P<0.05). Compared with the non-transfected cells in the control group, the N-2a cells with endogenously overexpressed GAL were arrested at the G0/G1 phases, and the over-expressed GAL protein significantly induced the N-2a cell apoptosis in a concentration-dependent fashion.

CONCLUSIONEukaryotic expression vector PcDNA 3.1-PDGF-GAL can encode the expression of GAL in N-2a cells. Aslo, it can inhibit cell proliferation and promote the cell apoptosis.

Animals ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Galanin ; biosynthesis ; Mice ; RNA, Messenger ; biosynthesis

Sleep is not just a rest for brain activity during daytime, but also has a vital function for memory consolidation after learning as well as restoration of both body and brain. While restoration of the body mainly occurs during non-rapid eye movement (NREM) sleep, especially during slow wave sleep, restoration of brain and memory consolidation occurs mainly during REM sleep. Adenosine acts as a sleep-inducing agent, so called somnogen or hypnotoxin which accumulates while awake. Sleep deprivation results in the disruption of every aspect of physical, cognitive, and behavioral function, which can be reversed only by sleep. Many neurotransmitter-secreting nuclei in the brain stem, hypothalamus, and basal forebrain are key structures for wakefulness, NREM, and REM sleep. They have been localized in the basal forebrain (acetylcholine), ventrolateral preoptic area (VLPO, GABA and galanin), tuberomamillary nucleus (TMN, histamine), lateral and posterior hypothalamus (orexin/hypocretin), reticular formation (glutamate), substantia nigra/ventral tegmental area (SN/VTA, dopamine), pedunculopontine nucleus and lateral dorsal tegmentum (PPT-LDT, acetylcholine), locus ceruleus (norepinephrine), and the raphe nuclei (serotonin). All are activated during wakefulness except VLPO which secrets GABA and galanin, which suppress other nuclei for sleep induction. Acetylcholine-secreting PPT-LDT is a major locus for REM sleep, and is inhibited by the raphe nuclei and locus ceruleus which act as REM-off neurons inducing NREM sleep. The suprachiasmatic nucleus is a pacemaker for circadian rhythms, which can be modified by bright light and melatonin. It should be emphasized that the best performance of cognitive function including reactivity, abstract thinking, creativity, memory, executive function, and accurate and efficient work as well as physical well-being is achieved by sufficient and appropriate sleep.
Adenosine ; Adolescent ; Brain ; Brain Stem ; Child ; Circadian Rhythm ; Creativity ; Executive Function ; Eye Movements ; Galanin ; gamma-Aminobutyric Acid ; Humans ; Hypothalamus ; Hypothalamus, Posterior ; Learning ; Light ; Locus Coeruleus ; Melatonin ; Memory ; Neurons ; Preoptic Area ; Prosencephalon ; Raphe Nuclei ; Reticular Formation ; Sleep Deprivation ; Sleep, REM ; Suprachiasmatic Nucleus ; Thinking ; Wakefulness

Adolescent ; Anticonvulsants ; therapeutic use ; Body Mass Index ; Child ; Child, Preschool ; Epilepsy ; blood ; drug therapy ; Female ; Galanin ; blood ; Humans ; Infant ; Male ; Valproic Acid ; blood ; therapeutic use

OBJECTIVETopiramate is a new broad-spectrum anti-epileptic drug. Decreased body weight and appetite are common side effects of topiramate. The side effect affects the growth and development in children greatly. Little is known about the mechanisms of topiramate-induced weight loss and decreased appetite in children with epilepsy in China and abroad. galanin is one of factors that affect appetite. It is a neuroendocrine peptide and play an important role in the control of appetite and body weight in the mechanism of hormone release. The purpose of this study was to explore the mechanism of topiramate-induced weight loss in children with epilepsy and the relation of weight loss with change of galanin, thereby to provide evidences for improvement of quality of life, compliance to treatment and reduce side effects of growth and development in children with epilepsy.

METHODSTotally 61 patients with especial epilepsy were enrolled into this study and the disease was defined by clinical manifestations and electroencephalography (EEG). Among them 32 cases had generalized seizures and 29 had local seizures. Sixteen normal children were enrolled as control group. The patients' age ranged from 0.5 to 14 (4.76 +/- 4.05) years and the patients were instructed to take 0.5 - 1 mg/kg of topiramate per day, with 0.5 - 1 mg/kg every 3 - 5 d increased to maximum of 3 - 8 mg/kg per day. Patients continued receiving the doses for 4 months. All patients' serum galanin levels and body height and weight and hepatic function were detected before and after antiepileptic drugs treatment. The galanin was detected by using radioimmunoassay.

RESULTSAfter treatment with topiramate (61 cases) for 4 months, plasma galanin [(22.01 +/- 8.12) pg/ml] declined as compared with baseline [(26.56 +/- 9.35) pg/ml, t = 2.85, P < 0.01] in children with epilepsy. Twenty-two of 61 patients lost weight, their plasma galanin concentration was significantly lower [(26.51 +/- 10.00) pg/ml vs. (20.45 +/- 8.09) pg/ml, t = 2.91, P < 0.01], but there was no significant change in the weight-gained patients (39/61) and control group (n = 16). In children with epilepsy, the mean value of body weight decreased as compared with the pre-treatment values, but the difference was not significant; however, the body-mass index (BMI) was significantly lower than that obtained before treatment (t = 8.628, P < 0.01). Eighteen of 22 patients who lost weight had decreased appetite, but only five of 39 patients who gained weight showed decreased appetite (chi(2) = 28.50, P < 0.001). The mean value of plasma galanin declined after treatment in patients (23 cases) with decreased appetite [(18.35 +/- 7.80) pg/ml vs. (27.28 +/- 6.90) pg/ml, t = 4.84, P < 0.001]; while plasma galanin did not change significantly after treatment in patients (38 cases) without decreased appetite [(24.23 +/- 7.66) pg/ml vs. (26.12 +/- 5.49) pg/ml, t = 1.04, P > 0.05].

CONCLUSIONTopiramate treatment may lower the body weight and reduce appetite in part of children with epilepsy which may be mediated by the reduced plasma galanin level.

Adolescent ; Anticonvulsants ; therapeutic use ; Appetite ; drug effects ; Case-Control Studies ; Child ; Child, Preschool ; Epilepsy ; drug therapy ; Female ; Fructose ; analogs & derivatives ; therapeutic use ; Galanin ; blood ; Humans ; Infant ; Male ; Weight Loss ; drug effects

To construct an immortalized rat astrocyte strain genetically modified by rat preprogalanin gene (IAST/GAL) and detect its galanin (GAL) expression and secretion, a cDNA fragment of rat GAL in plasmid of pBS KS(+)-GAL was inserted into eukaryotic expression vector pcDNA3.1 (+) by DNA recombinant technology, then the restriction enzyme digestion and DNA sequencing were carried out to evaluate the recombinant. The pcDNA3.1 (+)-GAL and pcDNA3.1 (+) construct were transfected into immortalized rat astrocyte strain (IAST) by lipofectamine and the population of cells which stably integrated the construct was selected with 600 microg/mL G418. Individual clones were screened and expanded into clonal cell strains. Detection of Neo gene was used to validate the success of the transfection. Immunocytochemical staining, RT-PCR and radioimmunoassay were used to detect the expression and secretion level of GAL. The recombinant had been successfully constructed by restriction enzyme digestion and DNA sequencing. Detection of Neo gene showed that the pcDNA3.1 (+)-GAL and pcDNA3.1 (+) have been successfully transfected into IAST. After selection by using G418, IAST/GAL and IAST/Neo cell strains were obtained. IAST/GAL, IAST/Neo and IAST were immunostained positively for GAL, but the GAL average optical density of IAST/GAL was significantly higher than that of IAST/Neo and IAST (P< 0.01). The level of GAL mRNA expression and the supernatant concentration of GAL in cultured IAST/GAL were significantly higher than those of IAST and IAST/Neo (P<0.01), but no significant differences were found between the IAST and IAST/Neo (P>0.05). It was concluded that IAST/GAL strain was constructed successfully and it might provide a basis for the further study of pain therapy.
Astrocytes/cytology ; Astrocytes/*metabolism ; Cell Line, Transformed ; Cells, Cultured ; Galanin/*biosynthesis ; Galanin/genetics ; Genetic Vectors ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/genetics ; Transfection

Animals ; Galanin ; administration & dosage ; antagonists & inhibitors ; pharmacology ; Patch-Clamp Techniques ; Peptide Fragments ; administration & dosage ; pharmacology ; Rats ; Rats, Wistar